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what composes total energy expenditure
basal metabolic rate; cost of keeping us alive
voluntary activity
thermic effect of food; cost of making food into a product that the body can use
proportions of BMR, activity and TEF in TEE
BMR is the largest, taking up to about 75%
activity is about 15%
TEF is about 10%
which is the easiest vs hardest to measure
activity is the most straightforward to measure
TEF is the hardest to measure due to being multifactorial
what factors affect TEF
meal size
meal composition (there is higher TEF for proteins and carb vs lipids)
meal frequency, timing, education
factors that can affect BMR can also affect TEF such as body composition, age, etc.
difference in TEF between obese vs lean individuals
TEF seems to be reduced in obese individuals as there seem to be small increase in metabolic rate compared to lean individuals when eating
factors that affect basal metabolic rate
height and weight= BMI
sex (%fat vs muscle mass [decrease BMR for fat vs muscle; more fat in women than men], hormones)
age/development/lifestage (pregnancy, lactation, infancy, childhood, adolescence, adulthood, senior)
hormone levels such as thyroid hormone
stress, fever, illness
other genetic factors
effects of medication and other compounds such as caffeine
fed, fasted or starved energic state
external and internal cues for energy intake
external cues
time of day
food availability
food quality
social norms and influences
internal cues
hunger and satiety
emotions such as stress or boredom
ghrelin
hunger hormone- produced by stomach increases drive to eat
vagus nerve
connects brain and digestive system (PSNS). stimulation by stretching the stretch receptors decreases appetite
leptin
energy expenditure hormone- is a protein hormone made by adipocytes. its levels correlate with energy reserves (stored triglycerides). leptin inhibits hunger, to stimulate satiety
GLP-1 (glucagon-like peptide-1)
produced by the large intestine and ileum. decreases blood glucose by increasing insulin and decreasing glucagon and decreases appetite by slowing gastric emptying
CCK (cholecystokinin)
peptide hormone that stimulates the digestion of fat and protein. secreted by duodenum in the small intestine
insulin
peptide hormone secreted by beta-cells in the pancreas. induces uptake of glucose into body cells (+other functions), reduces hunger
what is involved in anticipatory signaling
GLP 1 peaks 1 hour before a meal returns to baseline by meal start
ghrelin builds over time and declines with feeding
insulin increases just before mealtime and in response to blood glucos
obesity is affected by what factors
increases with age
lower risk with increasing education
lower risk in landed immigrants vs non immigrants due to cultural factors
dietary pattern (5+ fruits or vegetables per day reduces the risk)
obesity and T2DM relationship
chronic inflammation contributes to the development of insulin resistance in tissues
larger adipocytes in obesity attract macrophages by secreting macrophage chemotaxis protein
macrophages produces pro inflammatory TNFa
TNFa induces export of FFA into the blood leading to increased FFA in body
muscle imports the excess FFA from the blood, which builds up as ectopic lipid droplets by embedding themselves in muscles
ectopic lipid droplets interfere with GLUT-4 translocation leading to insulin resistance
increased use of FFA=increased toxic byproducts; damage to beta-cells of pancreas and insulin insufficiency
obesity and CVD
obesity increases the risk of dyslipidemia; high TG, high VLDL, high LDL and low HDL
LDL can penetrate vessel walls, become oxidized and form a plaque
high levels of VLDL in obesity prevent normal metabolism of lipoproteins, leading to abnormal transfer of cholesterol and triglycerides between lipoproteins
production of new lipoproteins enriched with triglycerides (VLDL-TG and LDL-TG). enriched lipoproteins can be converted into small dense-LDL (sd-LDL) by hepatic lipase
sd-LDL is like normal LDL but worse- better at penetrating artery walls, longer residence time in the blood, more susceptible to oxidation
limits of BMI as a measurement
muscle weighs much more than fat, so muscular individuals have higher BMI than expected
it only considers weight and heigh
does not factor in lean muscle mass vs adipose tissue
does not consider location of adipose tissue (visceral vs subcutaneous) varies across subpopulations and subcutaneous better predicts some comorbidities
ignores metabolic markers of disease risk and mental health component of obesity
alternative to BMI
EOSS (Edmonton obesity staging system)
more comprehensive rating scale that includes physical and psychological symptoms as well as functional limitations
focuses on associated health problem and their severity vs weight
stages of EOSS
stage 0= obese, but no risk factors present, no action or preventative options only
stage 1= subclinical risk factor(s) present, preventative options only
stage 2+= at least one established risk factor; specific nutritional, lifestyle, surgical and/or pharmacological action needed
lifespan of adipose cells
9.5 years
weight cycling
weight loss = decreased leptin = increased energy intake and decreased energy expenditure
BMR decreases
activity decreases
making it easier to regain positive energy balance, allowing adipose cells to refill
weight gain= increased leptin = decreased energy intake and increased energy expenditure
behavioural modification
may include CBT or cognitive behavioural therapy
preparatory phase= assess the nature and severity of obesity and any medical or psychosocial comorbidities
phase 1= initial weight loss including changing eating patterns, activity
phase 2= long-term weight maintenance phase focusing on locking in new habits, tapering off monitoring
general recommendations for dietary modification
high protein to promote satiety
water as a drink of choice
nutrient dense as opposed to energy dense food
reduced processed foods
substitutions as opposed to eliminations
fad diets
is a plan that promotes results such as fast weight loss without robust scientific evidence to support its claim
weight loss pharmacotherapy
orilstat- pancreatic lipase inhibitor limits fat absorption
liraglutide and semaglutide- GLP1 agonist reducing appetite
naltrexone and bupropion- hunger suppression
side effects
headache
dizziness
fatigue
GI disruption
hypoglycemia
gallbladder problems
pancreatitis
weight loss surger
gastric band
gastric bypass
sleeve gastrectomy
DSM-5TR of feeding and eating disorder
a disorder characterized by a persistent disturbance of eating or eating-related behaviour that results in the altered consumption or absorption of food and that significantly impairs physical health or psychosocial functioning
causes of feeding and eating disorder
multifactorial
psychological and sociocultural combine to develop a distorted body image
genetics can play with traits such as perfectionism and the baseline body type, hunger and satiety
changing social pressures
anorexia nervosa
persistent restriction of energy intake that leads to significant low body weight
bulimia nervosa
repeated binging episodes with a feeling of lack of control overeating and repeated compensation after eating by vomiting, misuse of laxatives, or excessive exercise to prevent weight gain
binge eating disorder
repeated binging episodes with a feeling of lack of control overeating but not repeated compensation after eating by vomiting, misuse of laxatives, or excessive exercise to prevent weight gain
anorexia athletica
eating disorder characterized by excessive and compulsive exercise which is particularly high in sports where a thin body is preferred- figure skating, ballet, gymnastics, dancing, skiing and other events
female athlete triad
disordered eating due to pressure to maintain lean, thin and athletic bodies leading to
energy restriction paired with excessive exercise can upset hormonal balance
low estrogen levels can lead to amenorrhea
low food intake and low estrogen can impact nutrient intake especially calcium